• 제목/요약/키워드: Smoke exposure

검색결과 209건 처리시간 0.028초

우리나라 성인 중 비흡연자에 대한 코티닌 노출수준 및 영향요인 분석 - 국민환경보건 기초조사(2009-2017) 결과 - (Urinary Exposure Levels of Cotinine and Influence Factors among Non-smokers in Korean Adults - Korean National Environmental Health Survey (2009-2017) -)

  • 전혜리;홍수연;주영경;권영민;정선경;이철우;유승도;유지영
    • 한국환경보건학회지
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    • 제46권2호
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    • pp.214-223
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    • 2020
  • Objectives: The aim of this study is to identify temporal trends in urinary cotinine levels and exposure factors among Non-smokers in Korean adults. Methods: Biological samples and questionnaire data were collected from representative Korean adults recruited in the Korean National Environmental Health Survey from 2009 to 2017. Multiple regression analysis was performed to determine the factors affecting urinary cotinine concentrations of non-smokers. Results: The urinary cotinine levels of Korean non-smokers decreased in Cycle 2 (1.04 ㎍/L, 2012-2014) compared to Cycle 1 (1.93 ㎍/L, 2009-2011) but increased slightly in Cycle 3 (1.37 ㎍/L, 2015-2017). Among the diverse variables, the main factors of cotinine exposure were secondhand smoke exposure and the presence of smokers in the family. Conclusions: The results of this study identified temporal trends in cotinine exposure among non-smokers in the Korean adult population. These findings will be used to develop further assessment and environmental health policies on secondhand smoke exposure.

The Relation between Exposure to Environmental Tobacco Smoke and the Quantity of Cotinine in the Urine of School Children in Taif City, Saudi Arabia

  • Desouky, Dalia El Sayed;Elnemr, Gamal;Alnawawy, Ali;Taha, Azza Ali
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권1호
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    • pp.139-145
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    • 2016
  • Environmental tobacco smoke (ETS) is a major public health problem for all ages. Despite the high prevalence of smoking among the Saudi population, there is limited information about levels of urinary cotinine in Saudi children exposed to SHS. The aim of the study was to assess the exposure of schoolchildren to ETS, and measure their urinary cotinine levels. Multistage cluster sampling was carried out, where schoolchildren from 4 schools were randomly chosen from primary schools in Taif city. A questionnaire including questions on SHS exposure and smoking rules in the residence were sent to students parents/guardians. Urine samples were taken and analyzed for total cotinine using chemiluminescent immunoassay. Of the studied children, 38.4% had a smoking father, 61.8%, 41.2% and 49.3% of them were exposed to ETS indoors, outdoors and both indoors and outdoors respectively. The mean urinary cotinine was significantly higher among children exposed to ETS compared to unexposed children. Urinary cotinine levels in children with both indoor and outdoor exposure was significantly higher compared with its level in children with single exposure. A significant positive correlation was found between urinary cotinine concentrations and the number of cigarette packs smoked by parents, and the number of smokers in the residence. The mean urinary cotinine level was significantly higher in children who reported no smoking rules at the residence.. The study revealed a high exposure of Saudi children to ETS. An antismoking media awareness campaign on the harmful effects of ETS should be carried out, in addition to family counseling programs targeted to parents to protect their children from ETS.

Pine bark extract (Pycnogenol®) suppresses cigarette smoke-induced fibrotic response via transforming growth factor-β1/Smad family member 2/3 signaling

  • Ko, Je-Won;Shin, Na-Rae;Park, Sung-Hyeuk;Kim, Joong-Sun;Cho, Young-Kwon;Kim, Jong-Choon;Shin, In-Sik;Shin, Dong-Ho
    • Laboraroty Animal Research
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    • 제33권2호
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    • pp.76-83
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    • 2017
  • Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of $Pycnogenol^{(R)}$ (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in $TGF-{\beta}1$/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

Impact of perinatal environmental tobacco smoke on the development of childhood allergic diseases

  • Yang, Hyeon-Jong
    • Clinical and Experimental Pediatrics
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    • 제59권8호
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    • pp.319-327
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    • 2016
  • Allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergy, are most common chronic, noncommunicable diseases in childhood. In the past few decades, the prevalence has increased abruptly worldwide. There are 2 possible explanations for the rising prevalence of allergic diseases worldwide, that an increased disease-awareness of physician, patient, or caregivers, and an abrupt exposure to unknown hazards. Unfortunately, the underlying mechanisms remain largely unknown. Despite the continuing efforts worldwide, the etiologies and rising prevalence remain unclear. Thus, it is important to identify and control risk factors in the susceptible individual for the best prevention and management. Genetic susceptibility or environments may be a potential background for the development of allergic disease, however they alone cannot explain the rising prevalence worldwide. There is growing evidence that epigenetic change depends on the gene, environment, and their interactions, may induce a long-lasting altered gene expression and the consequent development of allergic diseases. In epigenetic mechanisms, environmental tobacco smoke (ETS) exposure during critical period (i.e., during pregnancy and early life) are considered as a potential cause of the development of childhood allergic diseases. However, the causal relationship is still unclear. This review aimed to highlight the impact of ETS exposure during the perinatal period on the development of childhood allergic diseases and to propose a future research direction.

단세포전기영동법으로 평가한 흡연자의 백혈구 DNA손상 (Smoking Related DNA Damage in Human Lymphocytes Assessed by the Comet Assay)

  • 선수진;정해원;한정호
    • 한국환경성돌연변이발암원학회지
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    • 제22권2호
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    • pp.83-89
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    • 2002
  • The single cell gel electrophoresis (comet) assay is one of the useful tools for the study of genetic damage in humans exposed to environmental mutagens and carcinogens. This study was undertaken to evaluate the status of DNA damage in peripheral lymphocytes depending on their sex, age, smoking habits, and other factors in normal healthy Korean population. The 99 volunteers included in the study and out of these, 36 volunteers were smoker and 63 volunteers were non-smoker aged between 20-59 years. All individual answered a questionnaire that assessed their general information including smoking habits and the extent of the environmental tobacco smoke (ETS) exposure, and blood samples were obtained. There was a statistically significant difference in the extent of DNA damage between smoker and non-smoker (p<0.001). A significant difference was also observed between male and female (p<0.001) and amongst the different group of age (p<0.005), however, correlation analysis showed that only smoking habit was a significant factor for DNA damage. No significant effect of smoking duration, number of cigarettes smoking a day, SPY (smoke pack years) in smokers and environmental tobacco smoke exposure in non-smokers on the status of DNA damage was observed.

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Evaluating the Influence of Side Stream Cigarette Smoke at an Early Stage of Non-Alcoholic Steatohepatitis Progression in Mice

  • Kim, Jong Won;Yun, Hyejin;Choi, Seong-Jin;Lee, Sang-Hyub;Park, Surim;Lim, Chae Woong;Lee, Kyuhong;Kim, Bumseok
    • Toxicological Research
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    • 제33권1호
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    • pp.31-41
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    • 2017
  • Side stream cigarette smoke (SSCS) is known to be as harmful and hazardous to human health as is active smoking. In this study, we investigated the relationship between the exposure to SSCS and its stimulatory and subacute effects on the progression of non-alcoholic steatohepatitis (NASH). A methionine and choline-deficient plus high fat (MCDHF) diet was administered to C57BL/6 mice for 6 weeks. During the first three weeks of MCDHF diet feeding, each diet group was exposed to SSCS (0, 20, $40{\mu}g/L$) or fresh air for 2 hrs per day and 5 days per week. Additional experiments were performed by increasing the concentration (0, 30, $60{\mu}g/L$) and exposure time (6 hours per day) of SSCS. According to histopathologic analysis and serum levels of Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), there were no differences in hepatic fat deposition, fibrosis, apoptosis or liver damage in MCDHF-fed mice based on SSCS exposure. There were also no differences in the expression of inflammation-, oxidative stress- or fibrosis-related genes between MCDHF-fed mice with or without SSCS exposure. Therefore, it is concluded that SSCS with current exposure amounts does not have additive detrimental effects on the early stage of NASH.

환기(換氣)가 불량(不良)한 실내(室內)에서의 간접흡연(間接吸煙)에 관(關)하여 (Passive Smoking in Poorly Ventilated Room Space)

  • 이정애
    • Journal of Preventive Medicine and Public Health
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    • 제14권1호
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    • pp.23-31
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    • 1981
  • This study was conducted to investigate the effects of passive inhalation of cigarette smoke and the correlation between change of flicker value and active or passive smoking in poorly ventilated room. Forty five male students were tested by divided into four experimental groups composed of active and passive smokers and three control groups. Each four experimental groups were exposed to smoke for Two hours in enclosed room. Vital capacities, flicker values, blood carboxyhemoglobin levels and carbon monoxide concentration in room air were estimated before, during and after the exposure, and amounts of smoking or smoke exposure during two hours were also noted. The results obtained were as follows; 1. Concentration of carbon monoxide in air and increase of blood carboxyhemoglobin level (% COHb) were positively correlated with smoking amount. 2. Increase of blood carboxyhemoglobin in passive smokeres, in average, were about seventy six percent of that in smokers, as 2.2% vs. 2.9%. 3. Comparison with published data showed that Peterson's equation gave most similar result to this study in estimation of increase of blood carboxyhemoglobin level. 4. During the exposure, flicker values fell steadily in both experimental groups and control groups as time passed. Flicker values were, however, elevated again in experimental groups after exposure, despite the fact that values still fell in control groups. 5. Blood carboxyhemoglobin and flicker value were negatively correlated and this correlationship was stronger in passive smoker than in active smoker. 6. Multiple regression equation between flicker value and exposure time and blood carboxyhemoglobin level was expressed as: Flicker value=41.6-0.2 COHb%-0.9Hour, 7. In general, it is suggested that biological criteria would be more preferrable than chemical criteria in establishment of statutory limitation of smoking in enclosed spaces.

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Identification of Specific Gene Modules in Mouse Lung Tissue Exposed to Cigarette Smoke

  • Xing, Yong-Hua;Zhang, Jun-Ling;Lu, Lu;Li, De-Guan;Wang, Yue-Ying;Huang, Song;Li, Cheng-Cheng;Zhang, Zhu-Bo;Li, Jian-Guo;Xu, Guo-Shun;Meng, Ai-Min
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권10호
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    • pp.4251-4256
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    • 2015
  • Background: Exposure to cigarette may affect human health and increase risk of a wide range of diseases including pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung fibrosis and lung cancer. However, the molecular mechanisms of pathogenesis induced by cigarettes still remain obscure even with extensive studies. With systemic view, we attempted to identify the specific gene modules that might relate to injury caused by cigarette smoke and identify hub genes for potential therapeutic targets or biomarkers from specific gene modules. Materials and Methods: The dataset GSE18344 was downloaded from the Gene Expression Omnibus (GEO) and divided into mouse cigarette smoke exposure and control groups. Subsequently, weighted gene co-expression network analysis (WGCNA) was used to construct a gene co-expression network for each group and detected specific gene modules of cigarette smoke exposure by comparison. Results: A total of ten specific gene modules were identified only in the cigarette smoke exposure group but not in the control group. Seven hub genes were identified as well, including Fip1l1, Anp32a, Acsl4, Evl, Sdc1, Arap3 and Cd52. Conclusions: Specific gene modules may provide better understanding of molecular mechanisms, and hub genes are potential candidates of therapeutic targets that may possible improve development of novel treatment approaches.

Influence of Maternal Environmental Tobacco Smoke Exposure Assessed by Hair Nicotine Levels on Birth Weight

  • Lee, Jungun;Lee, Dong-Ryul;Lee, Do-Hoon;Paek, Yu-Jin;Lee, Won-Chul
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권7호
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    • pp.3029-3034
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    • 2015
  • Background: While the perinatal outcomes of active maternal smoking are well documented, results of the effects of environmental tobacco smoke (ETS) exposure during pregnancy are inconsistent. We aimed to examine the effect of ETS exposure, assessed by maternal hair nicotine levels at $35^{th}$ week of gestation, on birth weight and the risk of small for gestational age (SGA) and low birth weight (LBW). Materials and Methods: A total of 871 non-smoking healthy pregnant women were recruited by one Korean hospital between 1 October 2006 and 31 July 2007. Hair samples were collected and anthropometric questionnaires administered at $35^{th}$ week of gestation. The primary outcome was birth weight and secondary outcomes were the risk of babies being SGA and LBW. Results: Log-transformed hair nicotine concentrations were inversely related with birth weight after adjusting for confounding variables (${\beta}=-0.077$, p=0.037). After stratifying hair nicotine levels by tertiles (T1, low [0.0-0.28 ng/mg]; T2, medium [0.29-0.62 ng/mg]; and T3, high [0.63-5.99 ng/mg]), the mean birth weight in each groups were 3,342g (T1) 3,296g (T2) and 3,290 g (T3), respectively. However the difference between groups was not statistically significant by analysis of co-variance (ANCOVA) adjusting for covariates (p=0.062). In logistic regression analysis, the risk of SGA was higher in the T3 (OR=1.59, 95%CI 1.05-2.42) than in the reference group (T1), after controlling for confounding variables. The risk of low birth weight (<2,500g, LBW) was not significantly higher (OR=1.44, 95%CI 0.95-2.19), but the risk of babies being below 3,000g birth weight was increased in the T3 group (OR=1.53, 95%CI 1.00-2.36) compared with that in the T1 group. Conclusions: Maternal ETS exposure during pregnancy was inversely related with birth weight. The risk of SGA increased in the highest ETS exposure group compared with in the low exposure group. To prevent ETS exposure during pregnancy, more comprehensive tobacco control policies are needed.